title: 3-Nitropropionic acid-induced depression of spinal reflexes involves mechanisms different from ischemia-induced depression.
abstract: Effect of 3-nitropropionic acid (3-NPA) and ischemia (glucose- and O(2)-free solution) on synaptic transmission in hemisected spinal cord from 4 to 8 day old rats was examined in vitro. Stimulation of a dorsal root (L3-5 segments) evoked monosynaptic (MSR) and polysynaptic reflex (PSR) potentials in the segmental ventral root. Superfusion of 3-NPA (0.17-3.4 mM) depressed the reflexes in a concentration- and time-dependent manner. At 3.4 mM of 3-NPA, the reflexes were abolished by 35 min. Time required to produce 50% depression (T-50) was around 170, 80, 40 and 17 min for MSR and 110, 70, 25 and 16 min for PSR at 0.17, 0.51, 1.7 and 3.4mM of 3-NPA, respectively. Ischemia also produced a time-dependent depression of reflexes and abolished them by 35 min and the T-50 values were around 18 min. Presence of creatine phosphate (10mM) in the superfusing medium did not alter the time course of 3-NPA-induced depression of reflexes but prolonged the ischemia-induced depression. dl-2-amino-5-phosphonovaleric acid (NMDA receptor antagonist; 10 microM) failed to block the 3-NPA (3.4 mM)-induced depression of reflexes, but blocked the ischemia-induced depression. The results indicate that 3-NPA-induced depression of spinal reflexes does not involve NMDA receptors and is different from ischemia-induced depression.
authors.affiliation: Department of Physiology, Institute of Medical Sciences, Banaras Hindu University, Varanasi 221005, UP, India.
authors.forename: Rajesh
authors.initials: R
authors.lastname: Gupta
authors.forename: Shripad B
authors.initials: SB
authors.lastname: Deshpande
mesh_terms: D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D003292:Convulsants / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005260:Female; D005947:Glucose; D066298:In Vitro Techniques; D007511:Ischemia / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D009574:Nitro Compounds / Q000494:pharmacology*; D010725:Phosphocreatine / Q000032:analysis; D011422:Propionates / Q000494:pharmacology*; D051381:Rats; D012018:Reflex / Q000187:drug effects / Q000502:physiology*; D012023:Reflex, Monosynaptic / Q000187:drug effects / Q000502:physiology; D013116:Spinal Cord / Q000187:drug effects / Q000502:physiology*; D013126:Spinal Nerve Roots / Q000187:drug effects / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology; D013997:Time Factors
chemical_list: D003292:Convulsants; D018691:Excitatory Amino Acid Antagonists; D009574:Nitro Compounds; D011422:Propionates; D010725:Phosphocreatine; D015763:2-Amino-5-phosphonovalerate; D005947:Glucose; C015392:3-nitropropionic acid